Download Free Medical Strabismus Amblyopia and Leukocoria PowerPoint Presentation

Strabismus Amblyopia and Leukocoria PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Strabismus, Amblyopia & Leukocoria" by Saeed Alwadani, MD.

This medical PowerPoint presentation is about strabismus, amblyopia, and leukocoria, three eye conditions that can affect children and adults.

Strabismus, also known as crossed eyes, is a condition in which the eyes do not line up in the same direction. This can cause problems with depth perception and can lead to double vision. Strabismus can be caused by a variety of factors, including problems with the muscles that control eye movement or problems with the nerves that control those muscles.

Amblyopia, also known as lazy eye, is a condition in which one eye does not develop normal vision during early childhood. This can be caused by a variety of factors, including strabismus, unequal refractive error between the two eyes, or a blockage of vision in one eye. If left untreated, amblyopia can lead to permanent vision loss in the affected eye.

Leukocoria, also known as white pupil, is a condition in which the pupil appears white instead of black when light is shone into the eye. This can be caused by a variety of factors, including cataracts, tumors, or a condition called retinoblastoma, which is a type of eye cancer that typically affects young children.

All of these conditions can be diagnosed and treated by an ophthalmologist or optometrist. Treatment options can vary depending on the severity and cause of the condition, but may include glasses, eye patches, surgery, or other interventions. Its important to seek medical attention if you or your child experience any symptoms of these conditions.

Tags : Strabismus, Amblyopia, Leukocoria, ophthalmologist, optometrist, Pediatrics, Pediatrics PowerPoint presentation

Published on : Jun 23, 2023 | Views : 2219 | Downloads : 0

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Strabismus, Amblyopia & Leukocoria Saeed Alwadani, MD Assistant Professor Consultant Ophthalmologist Ophthalmology department King Saud University
Slide 2-

What is Strabismus ? Ocular misalignment due to abnormality in binocular vision or anomalies in neuromuscular control of ocular motility Strabismus has an inherited pattern, i.e., it is much more likely to occur if one or both parents are affected. However, many cases occur without any family history of the disorder
Slide 3-

Classification of Strabismus: According to fusion status Phoria Latent tendency of the eye to deviate and controlled by fusional mechanism Intermittent Phoria Fusion control is present part of the time Tropia Manifest misalignment of the eye all the time
Slide 4-

Classification of Strabismus: According to fixation Alternating Spontaneous alternation of fixation from one eye to the other Monocular Preference of fixation with one eye
Slide 5-

Classification of Strabismus: According to type of deviation Horizontal Esodeviation Exodeviation Vertical Hyperdeviation Hypodeviation Torsional Incyclodeviation Excyclodeviation Combined
Slide 6-

Classification of Strabismus: According to age of onset Congenital Acquired
Slide 7-

Classification of Strabismus: According to variation of the deviation with gaze position or fixing eye Comitant Same deviation in different direction of gaze Incomitant Variable deviation in different direction of gaze usually in paralytic or restrictive type of strabismus
Slide 8-

Examination History Inspection Assessment of monocular eye function Visual acuity Preverbal children CSM OKN Preferential looking Visual evoked potential
Slide 9-

Examination Assessment of monocular eye function Visual acuity Verbal children Symbol tests Single illiterate E Allen pictures H O T V letters
Slide 10-

Examination Assessment of binocular eye function Hirschberg test Krimski’s test(measuring) Cover test Alternate cover test Prism cover test
Slide 11-

Examination Fundoscopy Cycloplegic refraction Tropicamide Cyclopentolate Atropin
Slide 12-

Type of Strabismus Esotropia Pseudoesotopia Infantile esotropia Accommodative esotropia Partially accommodative esotropia
Slide 13-

Pseudoesotropia Occur in patients with flat broad nasal bridge and prominent epicanthal fold Gradually disappear with age Hirschberg test differentiate it from true esotropia
Slide 14-

Infantile Esotropia Common comitant esotropia occur before six month of age Deviation is often large more than 40 prism diopter Frequently associated with nystagmus and inferior oblique over action Treatment Correction of refractive error Treat amblyopia Surgical correction of strabismus
Slide 15-

Accommodative Esotropia Occur around 2 ½ years of age Start as intermittent then become constant High hypermetropia Treatment Full cycloplegic correction Treat amblyopia
Slide 16-

Partially Accommodative Esotropia Improve partially with glasses Treatment Full cycloplegic correction Treat amblyopia Surgical correction of strabismus
Slide 17-

Type of Strabismus Exotropia Intermittent exotropia Constant exotropia Sensory exotropia
Slide 18-

Intermittent exotropia Onset of deviation within the first year of age Closing one eye in bright light Usually not associated with any refractive error Usually not associated with amblyopia Treatment Correction of any refractive error Surgical correction of strabismus
Slide 19-

Constant exotropia Maybe present at birth or maybe progress from intermittent exotropia Treatment Correction of any refractive error Correction of amblyopia Surgical correction of strabismus
Slide 20-

Sensory exotropia Constant exotropia that occur following loss of vision in one eye e.g trauma Treatment Correction of any organic lesion of the eye Correction of amblyopia Surgical correction of strabismus
Slide 21-

Types of Strabismus Paralytic strabismus 6th nerve palsy 4th nerve palsy 3rd nerve palsy
Slide 22-

6th Nerve Palsy Incomitant esotropia Limitation of abduction Abnormal head position
Slide 23-

4th Nerve Palsy Congenital or acquired Hypertropia of the affected eye with excyclotropia Abnormal head position
Slide 24-

3rd Nerve Palsy Congenital or acquired Exotropia with Hypotropia of the affected eye In children caused by: trauma, inflammation, post viral and tumor In adult caused by: aneurysm, diabetes, neuritis, trauma, infection and tumor
Slide 25-

Special Types of Strabismus Duane strabismus Brown syndrome Thyroid opthalmopathy
Slide 26-

Duane Syndrome Limitation of abduction Mild limitation of adduction Retraction of the globe and narrowing of the palpebral fissure on adduction Upshoot or downshoot on adduction Pathology faulty innervation of the lateral rectus muscle by fibers from medial rectus leading to co-contraction of the medial rectus and lateral rectus muscles
Slide 27-

Brown Syndrome Limitation of elevation on adduction Restriction of the sheath of the superior oblique tendon Treatment needed in abnormal head position or vertical deviation in primary position
Slide 28-

Thyroid Ophthalmopathy Restrictive myopathy commonly involving inferior rectus, medial rectus and superior rectus Patients presents with hypotropia, esotropia or both
Slide 29-

Surgery of Extraocular Muscle Recession : weakening procedure where the muscle disinserted and sutured posterior to its normal insertion
Slide 30-

Surgery of Extraocular Muscle Resection : strengthening procedure where part of the muscle resected and sutured to its normal insertion
Slide 31-

Complication of Extraocular Muscle Surgery Perforation of sclera Lost or slipped muscle Infection Anterior segment anesthesia Post operative diplopia Congectival granuloma and cyst
Slide 32-

Amblyopia
Slide 33-

What is Amblyopia ?(Lazy Eye) Amblyopia refers to a decrease of vision, either unilaterally or bilaterally, for which no cause can be found by physical examination of the eye 2%–4% of U.S. population affected
Slide 34-

Amblyopia Three critical periods of human visual acuity development have been determined. During these time periods, vision can be affected by the various mechanisms to cause or reverse amblyopia. These periods are as follows: The development of visual acuity from the 20/200 range to 20/20, which occurs from birth to age 3-5 years. The period of the highest risk of deprivation amblyopia, from a few months to 7 or 8 years. The period during which recovery from amblyopia can be obtained, from the time of deprivation up to the teenage years or even sometimes the adult years
Slide 35-

Amblyopia Diagnosis of amblyopia usually requires a 2-line difference of visual acuity between the eyes
Slide 36-

Causes of Amblyopia Many causes of amblyopia exist; the most important causes are as follows: Anisometropia Inhibition of the fovea occurs to eliminate the abnormal binocular interaction caused by one defocused image and one focused image. This type of amblyopia is more common in patients with anisohypermetropia than anisomyopia. Small amounts of hyperopic anisometropia, such as 1-2 diopters, can induce amblyopia. In myopia, mild myopic anisometropia up to -3.00 diopters usually does not cause amblyopia.
Slide 37-

Causes of Amblyopia Strabismus The patient favors fixation strongly with one eye and does not alternate fixation. This leads to inhibition of visual input to the retinocortical pathways. Incidence of amblyopia is greater in esotropic patients than in exotropic patients Alternation with alternate suppression avoids amblyopia
Slide 38-

Causes of Amblyopia Visual deprivation Amblyopia results from disuse or understimulation of the retina. This condition may be unilateral or bilateral. Examples include cataract, corneal opacities, ptosis, and surgical lid closure Deprivation Amblyopia Bilateral Deprivation Amblyopia
Slide 39-

Causes of Amblyopia Organic Structural abnormalities of the retina or the optic nerve may be present. Functional amblyopia may be superimposed on the organic visual loss
Slide 40-

Causes of Amblyopia Ametropic Amblyopia Uncorrected high hyperopia is an example of this bilateral amblyopia.
Slide 41-

SCREENING: IMPORTANCE Amblyopia is usually preventable or treatable Early detection is key to effective treatment Life-threatening disorders may present as amblyopia Screening responsibility rests with primary care physician
Slide 42-

AMBLYOPIA: EARLY DETECTION Assess red reflex Determine visual acuity Evaluate ocular alignment
Slide 43-

Direct ophthalmoscope
Slide 44-

Direct ophthalmoscope: assessing red reflex
Slide 45-

Direct ophthalmoscope: examining retina
Slide 46-

Normal red reflex
Slide 47-

Asymetric red reflex
Slide 48-

Treatment The clinician must first rule out an organic cause and treat any obstacle to vision (eg, cataract, occlusion of the eye from other etiologies). Remove cataracts in the first 2 months of life, and aphakic correction must occur quickly Treatment of anisometropia and refractive errors must occur next The next step is forcing the use of the amblyopic eye by occlusion therapy
Slide 49-

ppt slide no 49 content not found
Slide 50-

Leukocoria A white pupillary reflex
Slide 51-

Leukocoria in a child requires urgent attention , primarily because in most patients with retinoblastoma it is the first sign noticed .
Slide 52-

Secondarily , a white pupil indicates a severely amblyopiogenic condition , which may be treatable . Anatomic location is important in the diffential diagnosis of Leukocoria
Slide 53-

Causes of Leukocoria Cataract Retinoblastoma Toxocariasis Coat´s disease ROP PHPV Retinal detachment Coloboma Retinal dysplasia Norrie´s disease
Slide 54-

Work –up 1- History 2- Complete ocular examination 3- B Scan ultrasonoghraphy 4- Intravenous fluorescein angiogram (coats disease , ROP, retinoblastoma ) 5- CT or MRI 6- Serum ELISA 7- Anterior chamber paracentesis 8-EUA
Slide 55-

opacification of the lens. Congenital cataracts usually are diagnosed at birth. cataract
Slide 56-

Unilateral cataracts are usually isolated sporadic incidents
Slide 57-

Bilateral cataracts are often inherited and associated with other diseases. They require a full metabolic, infectious, systemic, and genetic workup. The common causes are hypoglycemia, trisomy (eg, Down, Edward, and Patau syndromes), myotonic dystrophy, infectious diseases (eg, toxoplasmosis, rubella, cytomegalovirus, and herpes simplex [TORCH]), and prematurity
Slide 58-

RETINOBLASTOMA CLINICAL MANIFESTATIONS Leukocoria (60%) Strabismus (20%) OTHER- Uveitis, Orbital cellulitis, Hyphaema, Heterochromia, Glaucoma, Bupthalmos Retinoblastoma is the most common intraocular tumor of childhood.
Slide 59-

RETINOBLASTOMA
Slide 60-

Retinoblastoma Calcification is another feature of retinoblastomas, usually occurring in necrotic areas. Calcium stains with H&E. It is worth identifying calcium in suspect eyes by ultrasound, or CT scan to differentiate retinoblastomas from other tumours.
Slide 61-

MANAGEMENT EMPIRICAL GENETIC COUNSELLING ENUCLEATION unilateral, poor visual prognosis PLAQUE 4-12mm +/- vitreous seeding EXTERNAL BEAM >12mm, multiple foci, only eye LASER consider- indirect, xenon arc cryotherapy if <2dd in size CHEMOTHERAPY, if intracranial extension
Slide 62-

Persistent hyperplastic primary vitreous (PHPV) A gray-yellow retrolental membrane may produce leukocoria, with the subsequent suspicion of retinoblastoma. In PHPV, the globe is white and slightly microphthalmic. Patients have no history of prematurity or oxygen administration.
Slide 63-

RETINOPATHY OF PREMATURITY (ROP) Vasoproliferative retinopathy affecting premature infants exposed to high oxygen INCIDENCE Prematurity (<32/40) Birth weight (30% < 1000gm affected) Oxygen duration 90% ROP regresses spontaneously, 5% blindness
Slide 64-

Signs include: neovascularization, fibrous bands retinal detachments vitreous hemorrhage leukocoria RETINOPATHY OF PREMATURITY (ROP)
Slide 65-

ppt slide no 65 content not found
Slide 66-

COLOBOMA Optic Disc Coloboma Due to failure of closure of foetal fissure inferiorly May be isolated disc or associated chorioretinal coloboma Usually sporadic, some AD Can be bilateral Visual acuity varies from normal to NPL.
Slide 67-

THANKS FOR ATTENTION
Slide 68-

ppt slide no 68 content not found
Slide 69-

ppt slide no 69 content not found
Slide 70-

ppt slide no 70 content not found
Slide 71-

ppt slide no 71 content not found
Slide 72-

ppt slide no 72 content not found
Slide 73-

ppt slide no 73 content not found